Studies are described to further characterize the role of pulmonary afferents in the control of ventilation, by incorporating engineering control systems theory in the design and analysis of data from physiological and patho-physiological experiments. In initial studies we have investigated the positive feedback loop by which changes in vagal input lead to augmentation of phrenic nerve activity, and have demonstrated a relationship between the degree of augmentation and inspiratory airflow. Using this data and systems analysis we have developed the first known hypothesis on the function of this feedback loop, i.e., it reduces the delay between neural events in the medulla and changes in lung volume. We proposed a comprehensive investigation of the physiological function of this feedback loop and its disturbances in lung disease. Additionally we question which receptors are involved. Since others have recently demonstrated a relationship between the activity of the rapidly-adapting receptors (RAR) and airflow we hypothesize that RAR may mediate this feedback loop. Thus the RAR, which have been thought of as "irritant" receptors, may have a physiological role in ventilation. Indeed others have reached this conclusion although from different evidence. Thus we plan to initiate a general investigation of the role of RAR. We have developed a method of preferentially stimulating RAR using high frequency, small volume, oscillating airflow. Employing this technique we intend to establish the relationship between stimulation of the RAR and changes in respiratory neural output. In order to study how RAR may transduce airflow we propose relating changes in activity of individual receptors to changes in airway fluid mechanics. Existing information on the receptors' activity and location in the bronchial mucosa would suggest that they may respond to surface forces whose magnitudes are related to airflow. The magnitude of these forces will be altered by changes in the density and/or viscosity of the inspired gas. Finally the results of our studies will form a basis for a more general quantitative investigation of the interaction between different types of pulmonary vagal receptors in determining neural output in health and disease.